Saudi Journal of Kidney Diseases and Transplantation

: 1997  |  Volume : 8  |  Issue : 2  |  Page : 105--112

Acquired Cystic Renal Disease

Christopher R Blagg 
 Department of Medicine, Northwest Kidney Centers, Washington, USA

Correspondence Address:
Christopher R Blagg
Executive Director, Northwest Kidney centers, Seattle WA 98122

How to cite this article:
Blagg CR. Acquired Cystic Renal Disease.Saudi J Kidney Dis Transpl 1997;8:105-112

How to cite this URL:
Blagg CR. Acquired Cystic Renal Disease. Saudi J Kidney Dis Transpl [serial online] 1997 [cited 2021 Jun 19 ];8:105-112
Available from:

Full Text


Acquired cystic renal disease (ACRD) was first described in the kidneys of patients dying from Brights disease by John Simon in 1847 [1] , and again by Frerichs in 1851 [2] and by Piepers in 1894 [3] . It was re­discovered and reported in 1977 in a study of kidneys in hemodialysis patients [1] . While sometimes thought of as a complication occurring in dialysis patients, ACRD occurs as a consequence of damage produced by the underlying chronic kidney disease [4],[5],[6] ; dialysis merely lengthens the time over which cyst formation can occur.

Acquired cystic renal disease must be distinguished from other acquired renal cystic diseases such as the simple renal cysts that develop with advancing age, and the cystic changes found with primary hyper­aldosteronism that are probably related to hypokalemia. It also must be distinguished from hereditary autosomal-dominant poly­cystic disease, and from rare causes of cystic kidneys such as tuberous sclerosis, Von-Hipple-Lindau disease, autosomal­recessive polycystic disease, medullary cystic disease and medullary sponge kidney [7] .

Acquired renal cysts have been reported in some 7% to 22% of patients with chronic renal failure prior to starting on dialysis, and serial computerized tomography (CT) scans suggest that cysts start to develop when the serum creatinine level exceeds 365 µmol/L [8] . Cysts are found with increasing frequency as time on dialysis increases [9],[10] , and more than 80% of patients on dialysis for more than four years have developed cystic changes [9],[11] . Increasing numbers of cysts and enlarging kidney volume reflect the severity of ACRD [10] . Thus, the extent of cystic disease appears to relate to the duration and degree of uremia.

Acquired cystic renal disease is not specifically related to any one of the causes of chronic renal failure [11] , and may be commoner in males [9],[11],[12] and in black patients [11] . It also occurs in the kidneys of children on long-term dialysis [9],[11],[13],[14] at a frequency comparable to that seen in the adult patient population [15],[16] . While ACRD is often thought of as a complication found in hemodialysis patients, the incidence is similar in patients treated by long-term continuous ambulatory peritoneal dialysis (CAPD) [11],[17],[18] .

After successful kidney transplantation, ACRD may regress and the native kidneys atrophy, supporting the hypothesis that factors not removed by dialysis may be involved in its genesis [19] . However, in some cases presence of a functioning renal transplant may only slow progression of existing ACRD [11],[19],[20] , and as many as 18% of patients with a functioning trans­plant continue to show an increase in renal volume and number of cysts in their native kidneys despite good renal function [21] . In other cases, continuing increase in cysts may be related to poor function of the transplanted kidney and continuance of the cystogenic state [22] . Acquired renal cystic disease may occur more frequently in transplant recipients treated with cyclosporin [23] , and renal cell cancer, if it develops in such patients, may progress more rapidly, although this has not been the experience of others [24] .


Acquired cystic renal disease is characterized by development of fluid-filled cysts in the kidneys of patients with chronic renal failure due to non-cystic renal diseases. The cysts, usually between 3 mm and 5 cm in diameter, are lined with flattened/ cuboidal tubular epithelium and are mainly derived from the proximal tubules [6] . In the early stages of their development, the cysts are connected to an afferent and an efferent tubular segment through which a derivative of glomerular filtrate enters and leaves the cavity [25] . Once the cysts exceed some 2 millimeters in diameter, most detach from both portions of the renal tubule from which they are derived, and then the major source of cyst fluid is probably transepithelial secretion of sodium chloride and water. This may be stimulated by parathyroid hormone and possibly by other hormones. One or more retained uremic toxins also may act as growth factors that stimulate cystic transformation in the kidney [26] . Non-dialyzable mitogenic and cystogenic substances may accumulate, causing hypertrophy, hyperplasia and proli­feration of renal tubular epithelial cells in the surviving nephrons [11],[27] . The tubules are distorted by interstitial fibrosis [1] , and obstructed by hyperplastic epithelium and deposition of oxalate crystals, resulting in accumulation of fluid. At the same time, ischemia-induced parenchymal fibrosis results from occlusion of small blood vessels. The tubules dilate to form cysts, leading to an increase in kidney volume. In some patients the multifocal epithelial hyperplasia may progress to adenoma formation and even­tually to renal cell carcinoma, presumable by activation of certain oncogenes [11] .


Cysts are found in a number of renal diseases, suggesting that their formation can result from both inherited and acquired defects rather than being due to a single pathogenetic mechanism. Nevertheless, there is remarkable similarity of structure among cysts resulting from hereditary and acquired renal diseases. At least three components appear to be involved in cyst formation: increased epithelial cellular proliferation possibly resulting in intra­tubular obstruction, increased transepithelial fluid secretion, and abnormalities in the extracellular matrix [7] . In ACRD these may result from an insult to the mature kidney that results in de-differentiation [28] . Thus, cyst development in the scarred kidney of a patient with chronic renal failure resembles an extreme result of the intact nephron hypothesis as the tubules that survive the primary insult undergo hypertrophy and hyperplasia to form the cysts [29] .

There is also altered expression of various proto-oncogenes, growth factors and growth factor receptors such as c-myc, c-fos, c-Ki­ras, c-erb-B2, c-jun, transforming growth factor alpha, epidermal growth factor and epidermal growth factor receptor [27] , and epidermal growth factor precursor is found in the fluid of many varieties of renal cysts [30] . Increased sensitivity to epithelial growth factor and other mitogens found in the cyst fluid may be pathogenic for the development of progressive renal cystic disease.

Other suggested etiologic factors for ACRD include exposure to chemicals such as di-2-ethylhexylphthalate leached from the dialysis equipment, carcinogens in the dialysate water, formaldehyde, and accumu­lation of biologically active agents such as spermine, spermidine or putrescine in uremic plasma [31] . A possible role for chronic renal ischemia is suggested by a patient with a 13-year history of renal artery stenosis and a contracted left kidney who developed ACRD and renal cell carcinoma in the left kidney despite a serum creatinine level of only 168 µmol/L [32] .

 Clinical Manifestations and Diagnosis

Diagnostic screening for ACRD involves the use of renal ultrasonography and CT scanning. The former may be more helpful in the later stages, but CT scanning may be more sensitive when the kidneys and cysts are small [10],[11],[31] . The definitive imaging procedure after screening is contrast­enhanced CT scanning [33] or magnetic resonance imaging. Typically ACRD is bilateral, may begin before end-stage renal disease develops, and is usually asymptomatic and found accidentally during abdominal imaging.

If symptoms do occur, the most likely is pain due to hemorrhage into a cyst. This is more frequent in hemodialysis patients than in CAPD patients because of the repeated heparinization during dialysis [34],[35] . Retro­peritoneal hemorrhages and infections of the cysts can also occur. Sometimes the kidneys enlarge sufficiently to resemble autosomal-dominant polycystic kidney disease [36] , especially if one kidney has been removed previously [37] . Improvement of anemia in dialysis patients has been described in association with development of ACRD [38],[39],[40],[41] . This may be due to production of erythropoietin as a result of ischemia and interstitial hypoxemia from tissue compression. Significantly higher hematocrits have been found in patients with ACRD who have particularly large kidneys, although their erythropoietin levels were not different from those of patients with ACRD who had smaller kidneys and a lower hematocrit [42] .

 Renal Cell Carcinoma and ACRD

The most serious complication of ACRD is development of renal cell carcinoma [1],[6],[10],[20],[22],[43],[44],[45] , although the risk of developing this is present in dialysis patients both with and without ACRD [46] . In ACRD, the multifocal hyperplasia can lead to adenoma formation and thence to adenocarcinoma [47] . Parathyroid hormone is thought by some to stimulate neoplasia in association with both primary and secondary hyperparathyroidism [48] by activating adenylate cyclase and so, promoting sustained activation or mutation of one or more proto-oncogenes. This could result in transformation of cells and the development of malignancy. A proto-oncogene, C-erb B­2, that has been associated with breast and ovarian cancers is over-expressed in patients with end-stage renal disease, patients with ACRD, and patients with renal cell carcinoma. Other factors almost certainly also play a role in the development of neoplasia. For example, arginine vasopressin, VIP and adrenergic compounds may also increase the rate of fluid secretion by cysts.

A histopathologic and molecular genetic study of 21 renal cell carcinomas from dialysis patients found a preponderance of chromophilic renal cell carcinomas. Only a small number of these tumors showed the deletion of gene sequences in the short arm of chromosome 3 (3p), seen in almost all cases of the clear cell carcinoma that is the predominant type of renal cancer in the general population [49] . Thus, the genetic changes underlying development of renal tumors in patients with end-stage renal disease differ from those occurring with sporadic clear cell renal cell carcinoma. Chronic renal failure appears to promote structural chromosomal abnormalities including trisomy, and in a recently reported case, karyotype analysis showed trisomy of chromosomes 5,16 and 20 and deletion of chromosome Y. These cytogenetic changes are similar to those found in sporadic cases of renal cell carcinoma in the general population [50] . Perhaps, a genetic factor modulating tubular cell growth is affected by uremia, and this could account for a linkage between papillary hyperplasia and development of renal cell carcinoma [49] .

Renal cell carcinoma in a patient with ACRD may be asymptomatic in as many as 86% of cases, although in many of these the tumor is small and may still be considered an adenoma [51] . In those patients who develop symptoms, the commonest are due to bleeding into the tissue of the tumor [45] , into the renal parenchyma with rapid swelling of the kidney, into the subcapsular or retroperitoneal space with flank pain, or into the pyelocalyceal system resulting in gross hematuria. In some cases, persistent hematuria may be the only symptom and the cancer may not be detectable by the usual imaging procedures.

Screening by ultrasonography is useful and readily available, but small cysts and tumors may not be seen. Contrast-enhanced CT scanning shows the renal outlines and content more clearly. Especially with solid tumors, CT scanning may need to be supplemented with arteriography or magnetic resonance imaging [52] . Nevertheless, ACRD­related renal cell carcinomas may not be detected by imaging techniques and may manifest themselves only by kidney enlargement [53],[54] . The development of renal cancer appears to be correlated with kidney size, reflecting the volume of cysts and epithelial cell proliferation. Kidneys with ACRD weighing more than 150 gm are six-times more likely to contain cancer (56%) than are smaller kidneys (11%) [47] . This is in keeping with the view that the development of malignancy in patients with ACRD is a progressive process that starts in terminally differentiated renal tubules and progresses through adenoma to adeno­carcinoma [44],[47],[55] . Even so, as many as 17% of the renal cancers found in dialysis patients occur in the absence of ACRD [6],[11],[56] .

The reported frequency of renal cancer in dialysis patients varies widely and a recent review suggested a prevalence of 1.3 % in patients with ACRD [57]. A Japanese study found two cases of renal cell carcinoma in 57 patients over a ten-year period [58] , and a study in the United States found two cases of renal cell carcinoma in 30 patients over seven years [10] . This suggests the annual incidence of renal cell carcinoma in dialysis patients is some three to six times that in the general population [10],[59],[60] . Others have reported an incidence as high as 57 to 134 times that in the general population [12] .

A nationwide Japanese survey covering some 57,500 dialysis patients over a two­year period, found that renal carcinomas had been detected in 112 male and 18 female patients. Their average age was 52.6 years, and the mean duration on dialysis was 106 months [61] . The incidence rate was 125 cases per 100,000 patients, compared with 3 cases per 100,000 in the general population over a similar time period. Diagnosis was based on CT scan or renal ultrasonography in 83.6% of the affected patients; CT scan in 59 cases and ultra­sonography in 48 cases. Acquired cystic renal disease was present in 82.3% of the cases, bilateral renal cell carcinomas were found in 11 patients, and 19 patients (15.1%) had metastases. Curative nephrectomy was performed in 99 of 129 patients, the mean tumor diameter being 4.2 + 2.5 cm (range 0.5 to 15.0 cm). Perhaps this high incidence of tumors reflected the frequency of small (3 cm or less) renal tubular neoplasms that were adenomatous and might never have developed into clinically significant malignant lesions.

The incidence of tumors increases with time on dialysis and the severity of ACRD. They are four to seven times more common in males than in females [9],[11],[59] , and this compares with the two-fold greater risk of renal cancers in males compared with females in the general population of the United States. In general, ACRD-associated renal cell carcinoma occurs some 13 to 20 years earlier in dialysis patients than in the general population (45 ± 18 years vs. 64 ± 12 years) [60],[62] and has also been reported in association with ACRD in peritoneal dialysis patients [34],[51],[63] . Renal cell carcinoma in association with ACRD occasionally develops in pediatric dialysis patients [64] , in one case in a 13-year-old boy who had been on dialysis for nine years [14] . Whether there is a racial difference in the incidence of ACRD-associated renal cell carcinoma is unknown, although this may be more common in black patients in the United States. In Japanese patients the incidence resembles that in white patients [6] .

In as many as 86% of cases, renal cell carcinoma is asymptomatic, and it metasta­sizes in 20% or less of cases [6],[63],[65] . Annual CT screening of dialysis patients has been suggested [9] , but death from renal cell carcinoma is relatively rare in dialysis patients, most dying from cardiovascular causes. In fact, the 5-year survival rate for patients diagnosed as having cancer of the end-stage kidney is about 35%, similar to the 42% survival for the general population with renal cancer [10] . The major differences are that renal cancer associated with ACRD is more often bilateral and multifocal, and that non-papillary renal cell carcinomas are the common type in the general population, while papillary renal cell tumors are much more frequent in dialysis patients.

Long-term dialysis patients frequently have severe cardiovascular disease and are poor surgical risks for radical nephrectomy. Because a tumor found by screening may be small and asymptomatic [60] , routine screening of all dialysis patients might have little impact on patient survival [9] . Also, based on 1987 cost data, annual CT screening of dialysis patients in the United States beginning three years after they start on dialysis would add at least 36 million US dollars to the Medicare budget [10] . With the increasing numbers of dialysis patients each year and the increasing costs of health care, this figure would be much higher today.

The effects of screening have been examined by decision analysis modeling using a tumor growth model to provide estimates of the relationship between tumor size, clinical stage and patient survival. Three strategies were assessed; no screening until patients develop symptomatic cysts and/or cancer; CT screening or ultrasound screening starting three years after starting dialysis and annually thereafter in those found to have cysts; and every three years in patients without cysts. The benefit of screening was found to depend critically on the life expectancy of the patient [66] . For example, for a 20-year old non-diabetic patient starting dialysis with a 25-year life expe­ctancy, screening could increase this by about 1.6 years (6%). By comparison, for a 58 year-old patient starting dialysis with a life expectancy of five years, screening would only prolong life by four or five days (0.3%). Perhaps the best compromise is to screen young male dialysis patients who have been on dialysis for several years, are known to have ACRD, and have large kidneys [10],[12],[59] . The median age of patients starting dialysis in the United States is now more than 60 years, and diabetes is the cause of renal failure in more than one third of patients, suggesting that less than half the patients would benefit from screening. Sensitivity analysis also shows that if the false positive rate with screening techniques is 10%, this would result in an actual shortening of life expectancy for dialysis patients aged 64 and older. If this not unreasonable false positive rate applies, screening would actually shorten survival for almost half the dialysis patients in the United States.

The occurrence of hematuria, flank pain, unexplained fever or systemic illness in a dialysis patient is an indication for renal imaging. Until a subset of dialysis patients is identified for whom annual imaging is cost effective, the main consideration should be the general medical condition and life expectancy of the individual patient. Finding a renal carcinoma in an elderly patient with significant cardiovascular or other disease may have no effect on patient care and prognosis. On the other hand, a young, relatively fit dialysis patient may benefit greatly if renal imaging finds a renal tumor that is still localized to the kidney and is easily resectable. It may also be possible to assess prognosis by DNA flow cytometric analysis of the cellular DNA content and S­phase fraction. There appears to be a close relationship between DNA aneuploidy and high S-phase fraction and the tendency to metastasize or to develop recurrence [67] . There are also some differences in the DNA content profile of renal cancers in patients with ACRD compared with that in such tumors arising in the general population, perhaps reflecting differences in the biological nature of these neoplasms.

Renal cell carcinoma can also occur in the native kidneys of a patient some two to fifteen years after successful kidney transplantation [24],[68] . Most of these patients have metastases at the time of diagnosis and also have evidence of ACRD. Thus, the malignant potential of the proliferative changes of ACRD is not removed by trans­plantation, and immunosuppressive treatment, especially with cyclosporin [23] , may activate occult renal cancers. In one study, metastatic renal carcinoma accounted for 2% of deaths in kidney transplant recipients [69] . Consequently, the native kidneys of potential transplant recipients should be imaged by CT or ultrasound to exclude tumors as part of the pre-transplant work up [11] . It has also been suggested that screening be done annually in transplant recipients, as the malignant potential asso­ciated with ACRD persists even after many years of normal renal function [24] . Certainly, if a transplanted patient develops high risk factors such as gross hematuria, flank pain, fever or a puzzling systemic illness, their native kidneys should be imaged to exclude tumors. Screening should also be used in patients with any two of the following moderate risk factors: ACRD, more than four years on dialysis, male sex, and a history of a questionable renal mass [70] . If questionable renal masses are seen with CT scanning, serial examinations at regular intervals are indicated, and any renal tumor should be removed [33],[68],[70],[71],[72] .

In the United States there are now more than 250,000 dialysis patients, more than 60,000 new patients start treatment for end­stage renal disease each year, and more and more patients are living longer on dialysis [73] . More than 80% of dialysis patients have developed ACRD after four years on dialysis, and by 10 years this is present in all patients [11] . Consequently, the develop­ment of ACRD-associated renal cancers will become an ever-larger problem in future years.


1Dimnill MS, Millard PR, Oliver D. Acquired cystic disease of the kidneys: a hazard of long-term intermittent maintenance haemodialysis. J Clin Path 1977;30:868-77.
2Frerichs FT. Die Bright'sche Nierenkrankheit und deren Behandlung. Braunschweig: F. Vieweg und Sohn, 1851.
3Peipers A. Uebereine besondere Form von Nierensteinen. Munchen Med Wochenschrift 1894;41:531-32.
4Grantham JJ, Levine E. Acquired cystic disease: replacing one kidney disease with another. Kidney Int 1985;2S:99-105.
5Bretan PN Jr, Busch MP, Hricak H, Williams RD. Chronic renal failure: a significant risk factor in the development of acquired renal cysts and renal cell carcinoma. Case reports and review of the literature. Cancer 1986;57:1871-9.
6Ishikawa I. Acquired renal cystic disease. In: Gardner KDJ, Bernstein J, editors. The Cystic Kidney. Boston: Kluwer, 1990;351­-77.
7Fick GM, Gabow PA. Hereditary and acquired cystic disease of the kidney. Kidney Int 1994;46:951-64.
8Mickisch O, Bommer J, Bachmann S, Waldherr R, Mann JF, Ritz E. Multicystic transformation of kidneys in chronic renal failure. Nephron 1984;38:93-9.
9Ishikawa I. Acquired cystic disease: mechanisms and manifestations. Semin Nephrol 1991;11:671-84.
10Levine E, Slusher SL, Grantham JJ, Wetzel JH. Natural history of acquired renal cystic disease in dialysis patients: A prospective longitudinal CT study. Am J Roentgenol 1991; 156:501-6.
11Matson MA, Cohen EP. Acquired cystic kidney disease: Occurrence, prevalence and renal cancers. Medicine Baltimore 1990;69:217-26.
12Concolino G, Lubrano C, Ombres M, Santonati A, Flammia GP, Di Silverio F. Acquired cystic kidney disease: the hormonal hypothesis. Urology 1993;41:170-5.
13Hogg RJ. Acquired renal cystic disease in children prior to the start of dialysis. Pediatr Nephrol 1992;6:176-8.
14Gentle DL, Mandell J, Jennings T. Renal cortical neoplasm in a child with dialysis-acquired cystic kidney disease. Urology 1996;47:254-5.
15Leichter HE, Dietrich R, Salusky IB, et al. Acquired cystic kidney disease in children undergoing long-term dialysis. Pediatr Nephrol 1988;2:8-11.
16Sieniawska M, Roszkowska-Blaim M, Welc-Dobies J. Acquired cystic kidney disease in renal insufficiency. Child Nephrol Urol 1991; 11:20-4.
17Ishikawa I. Acquired renal cystic disease and its complications in continuous ambulatory peritoneal dialysis patients. Perit Dial Int 1992;12:292-7.
18Katz A, Sombolos K, Oreopoulos DG. Acquiredcystic disease of the kidney in association with chronic ambulatory peritoneal dialysis. Am J idney Dis 1987; 9:426-9.
19Ishikawa I, Yuri T, Kitada H, Shinoda A. egression of acquired cystic disease of the kidney after successful renal transplant­ation. Am Nephrol 1983;3:310-4.
20Levine E, Grantham JJ, Slusher SL, Greathouse JL, Krohn BP. CT of acquired cystic kidney disease and renal tumors in long-term dialysis patients. Am J Roentgenol 1984;142:125-31.
21Ishikawa I, Shikura N, Shinoda A. Cystic trans formation in native kidneys in renal allograft recipients with long-standing good function, Am J Nephrol 1991;ll:217-23.
22Ishikawa I, Shikura N, Kitada H, Yuri T, Shinoda A, Nakazawa T. Severity of acquired renal cysts in native kidneys and renal allograft with long standing poor function Am J Kidney Dis 1989;14:18-24.
23Lien YH, Hunt KR, Siskind MS, Zukoski C. Association of cyclosporin A with acquired cystic kidney disease of the native kidneys in renal transplant recipients. Kidney Int 1993;44:613-6.
24Heinz-Peer G, Schoder M, Rand T, Mayer G, Mostbeck GH. Prevalence of acquired cystic kidney disease and tumors in native kidneys of renal transplant recipients: a prospective US study. Radiology 1995;195:667-71.
25Grantham JJ. Pathogenesis of renal cyst expansion: opportunities for therapy. Am J Kid Dis 1994;23:210-8.
26Crocker JFS, Safe SH. An animal model of 42 hemodialysis induced polycystic kidney disease (PKD). (Abstract). Kidney Int 1984;25:183.
27Nadasdy T, Laszik Z, Lajoie G, Blick KE, Wheeler DE, Silva FG. Proliferative activity of 43 cyst epithelium in human renal cystic diseases. J Am Soc Nephrol 1995;5:1462-8.
28Grantham JJ. 1992 Homer Smith Award. Fluid secretion, cellular proliferation, and the pathogenesis of renal epithelial cysts. J Am Soc Nephrol 1993;3:1843-57.
29Grantham JJ. Acquired cystic kidney disease. Kidney Int 1991;40:I43-52.
30Moskowitz DW, Bonar SL, Liu W, Sirgi CF, Marcus MD, Clayman RV, growth factor precursor is present in a variety of human renal cyst fluids. J Urol 1995;153:578-83.
31Banyai-Falger S, Susani M, Maier U. Renal cell carcinoma in acquired renal cystic disease 3 years after successful kidney transplantation. Two case reports and review of the literature. Eur Urol 1995;28:7.7-80.
32Sinsky CA, Dahlberg PJ, O'Connor J. Unilateral acquired renal, cystic disease and neoplasia in a patient with renal artery stenosis. Urology 993;41:287-8.
33Marple JT, MacDougall M, Chonko AM. Renal cancer complicating acquired cystic kidney disease. J Am Soc Nephrol 1994;4:1951-6.
34Trabucco AF, Johansson SL, Egan JD, Taylor RJ. Neoplasia and acquired renal cystic disease in patients undergoing chronic ambulatory peritoneal dialysis. Urology 1990;35:l-4.
35Cotterell L, Egan JD, Wells IC, et al. Significant incidence of ACKD in CAPD patients. Perit Dial Bull 1986;6:S5 Abstract.
36Poulopoulos V, Bargman JM. Acquired cystic disease mimicking polycystic kidney disease in a long-term CAPD patient. Perit Dial Int 1995;15:75-6.
37Kessler M, Testevuide P, Aymard Acquired renal cystic disease mimicking adult polycystic kidney disease in a patient undergoing long-term hemodialysis. Am J Nephrol 1991;11:513-7.
38Goldsmith HJ, Ahman R, Raichura N, et al. Association between rising haemoglobin concentration and renal cyst formation in patients on long-term regular haemodialysis treatment. Proc EDTA 57 1982;19:313-8.
39Ono K, Kikawa K, Okamoto T, Matsuo H. Normalization of hematocrit in regular hemodialysis patients: the role of renal cyst formation. Trans Am Soc Artif Intern Organs 1985;31:639-43.
40Shalhoub RJ, Rajan U, Kim VV, Goldwasser E, Kark JA, Antoniou LD. Erythrocytosis in patients on long-term hemodialysis. Ann Intern Med 1982;97:686-90.
41Fernandez A, Hortal L, Rodriguez JC, Vega N, Plaza C, Palop L. Anemia in dialysis: its relation to acquired cystic kidney disease and serum levels of erythropoietin. Am J Nephrol 1991;11:12-5.
42Schillinger F. Acquired cystic kidney disease in renal insufficiency: a multicentre study. Group of Nephrologists of the East of France. Eur J Med 1993;2:457-60.
43Hughson MD, Buchwald D, Fox M. Renal neoplasia and acquired cystic kidney disease in patients receiving long-term dialysis. Arch Pathol Lab Med 19S6;110:592-601.
44Grantham JJ. Polycystic kidney disease: neoplasia in disguise. Am J Kidney Dis 1990;15:110-6.
45Truong LD, Krishnan B, Cao JT, Barrios R, Suki WN. Renal neoplasm in acquired cystic kidney disease. Am J Kidney Dis 1995;26:1-12.
46Herrera GA. C-erb B-2 amplification in cystic renal disease. Kidney Int 1991;40:509-13.
47MacDougall ML, Welling LW, Wiegmann TB. Prediction of carcinoma in acquired cystic disease as a function of kidney weight. J Am Soc Nephrol 199O;l:828-31.
48Kopple JD, Massry SG. Is there an association between neoplasia and primary or secondary hyperparathyroidism? Am J Nephrol I988;8:437-48.
49Hughson MD, Schmidt L, Zbar B, et al. Renal cell carcinoma of end-stage renal disease: a histopathologic and molecular genetic study. J Am Soc Nephrol 1996;7:2461-8.
50Ishikawa I, Shikura N, Ozaki M. Papillary renal cell carcinoma with numeric changes of chromosomes in a long-term hemodialysis patient: a karyotype analysis. Am J Kidney Dis 1993;21:553-6.
51Ishikawa I. Uremic acquired renal cystic disease. Natural history and complications. Nephron 1991;58:257-67.
52Ishikawa I. Uremic acquired cystic disease of kidney. Urology 1985;26:101-8.
53Gehrig JJ Jr, Gottheiner TI, Swenson RS. Acquired cystic disease of the end-stage kidney. Am J Med 1985;79:609-20.
54Cho C, Griedland GW, Swenson RS. Acquired renal cystic disease and renal neoplasms in hemodialysis patients. Urol Radiol 1984;6:153-7.
55Mendley SR, Toback FG. Cell proliferation in the end-stage kidney. Am J Kidney Dis 1990;16:80-4.
56Gardner KD Jr, Evan AP. Cystic kidneys: an enigma evolves. Am J Kidney Dis 1984;3:403-13.
57Glicklich D. Acquired cystic kidney disease and renal cell carcinoma: a review. Semin Dial 1991;4:273-83.
58Ishikawa I, Saito Y, Shikura N, Kitada H, Shinoda A, Suzuki S. Ten-year prospective study on the development of renal cell carcinoma in dialysis patients. Am J Kidney Dis 1990;l6:452-8.
59Levine E. Renal cell carcinoma in uremic acquired renal ' cystic disease: incidence, detection, and management. Urol Radiol 1992;13:203-10.
60Chandhoke PS, Torrence RJ, Clayman RV, Rothstein M. Acquired cystic disease of the kidney: a management dilemma. J Urol 1992;147:969-74.
61Ishikawa I. Renal cell carcinoma in chronic hemodialysis patients-a 1990 questionnaire study in Japan. Kidney Int Suppl 1993;41:S167-9.
62Hughson MD, Hennigar GR, McManus JF. Atypical cysts, acquired renal cystic disease, and renal cell tumors in end stage dialysis kidneys. Lab Invest 1980;42:475-­80.
63Master U, Schmidt R, Dumler F, Babiarz J. Renal malignancy in peritoneal dialysis patients with acquired cystic kidney disease. In: Khanna R, Nolph KD, Prowant BF, Twardowsli ZJ, Oreo-poulos DG, editors. Advances in Peritoneal Dialysis. Toronto: Peritoneal Dialysis Publications Inc. 1992:145-49.
64Querfeld U, Schneble F, Wradzidlo W, Waldherr R, Troger J, Scharer K. Acquired cystic kidney disease before and after renal transplantation. J Pcdiatr 1992;121:61-4.
65Spencer SJW, Philips ME. Transitional-cell carcinoma in acquired cystic disease of the kidney in a patient on CAPD. Nephrol Dial Transplant 1990;5:464-5.
66Sarasin FP, Wong JB, Levey AS, Meyer KB. Screening for acquired cystic kidney disease: a decision analytic perspective. Kidney Int1995;48:207-19.
67Mallofre C, Almirall J, Campistol JM, Andreu J, Cardesa A, Revert L. Acquired renal cystic disease in HD: a study of 82 nephrectomies in young patients. Clin Nephrol 1992;37:297-302.
68Levine LA, Gburek BM. Acquired cystic disease and renal adenocarcinoma following renal transplantation. J Urol 1994;151:129­-32.
69Dlugosz BA, Bretan PN Jr, Novick AC, et al. Causes of death in kidney transplant recipients: 1970 to present. Transplant Proc 1989;21:2168-70.
70Bretan PN Jr. Acquired renal cystic disease: is there a need for screening for renal cell carcinoma in patients with renal failure? Semin Urol 1994;12:89-92.
71Nakano E, Iwasaki A, Seguchi T, et al. Incidentally diagnosed renal cell carcinoma. Eur Urol 1992;21:294-8.
72Basile JJ, McCullough DL, Harrison LH, Dyer RB. End stage renal disease associated with acquired cystic disease and neoplasia. J Urol 1988;140:938-43.
73U.S. Renal Data System, USRDS 1996 Annual Data Report. 1996; Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases.